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Topic: Time to failure (Atripla) ? (Read 15850 times)

1) Assuming that someone have resistances (let say 103, 108, 141), how long time does it take in average before the regimen will fail ? Is there a period above what we can assume to not have resistances to this regimen (eg. 6 months ?)

In fact, my very first genotype was showing resistances, but not the 2 that has follow.And because of the presence of the 141 mutation, it was believe that the first genotype wasn't mine (as it should have disapear in the absence of drug pressure -and I was treatment naive).So my current regimen. I have been undetectable after 3 weeks and always since (but last lab made 3 weeks ago). I saw an increase of the CD4% of 3%, but my CD4 have remain almost unchanged (slight decrease to 530 for 570).

2) Looking at many CD4 counts here or there for people on Atripla, I believe that it is common to see at the begining of the treatment a slight drop in the CD4 count (but often an increase of the CD4%).Any explanations for that (death of the infected cells ?) ?

3)Assuming a virologic failure, would we get any sign of it, such as swollen lymphs node or so.So far, mine have almost disapear, but I am not sure if it is swolling a bit more or not. I guess no.

Why are you asking about "virologic failure" when you aren't sharing your Viral load from your tests? they aren't testing for viral loads? If you are undetectable count your blessings and think healthy thoughts for the future. why are you assuming failure?

Logged

“From each, according to his ability; to each, according to his need” 1875 K Marx

I go and see my ID Doc on 03/27. We will see if my cd4 count drops (Although I hope it doesn't). If it does I will asked a lot of questions and advise you of the responses if you would like. On 03/27, I will have been taking Atripla for about 40 days. I will give blood 7 days prior, therefore 33 days on Atripla for the purpose of calculating the effects of Atripla.

I have noticed something new in the past week. When I wake up each morning, I notice quite a bit of hair on my pillows. I am hoping this is not some sort of side effect. In any event, I do not want to loose my hair at any cost. This would be a deal breaker if it is realted to Atripla.

So far, I haven't fail on Atripla.I am just wondering how long time it will take to conclude definitely that my first genotype wasn't mine.It's a boring situation, just that, but indeed, I count my blessing to be so far undetectable !

Hi clsoca

If there is a drop at the begining, I can already tell you that it seems to be very common (for the first labs after starting HAART). I was interested to know why. I know some will call it a normal bounce, a measure error and so, but I guess it also have to do with the death of the infected cells (a CD4 counts doesn't distinguish those infected from those who are virus free). So the drop.That's my explanation, but I might be 200% wrong and maybe others know.Now over the time, we are all expecting that the trend will shows an increase

If you ask any questions to your doc, and post them with the answers you have get, you are more than very welcome. For the community and me too hehe

If you think about the biology of resistance, it probably matters. If only resistant to one drug and you have two others working, once you are undetectable the only source of virus is stuff released from reservoirs. And it seems unlikely that virus released from reservoirs would be able to overcome the working drugs and reproduce.

clsoca: Reservoirs are the reason that current HAART medications can't "cure" HIV. Soon after initial infection HIV establishes itself in certain cells throughout the body. When someone goes on HAART and they become undetectable, whatever small amounts of virus is in their system is coming from these reservoir cells (also called "sanctuary" cells).

ARV medication is not able to get to HIV in these cells. If they could, then HIV can be eradicated completely from the body. It's frustrating because it's actually a teeny tiny amount of virus. If someone who is on a successful regimen and undetectable goes off their meds this activates the latent HIV in these reservoirs to begin to reproduce and VL goes back up again, which is why for the time being HIV meds are a commitment for life. If scientists can find a way to "flush" out the HIV in the reservoirs, by getting them to reproduce and not lay dormant, the current available medications can kill it and that would rid the body of all HIV. (Yeeaaah@!)

When ARV medications first came on the scene in the mid to late 1990s, it was thought that if you take them for a few years (5 to 7 years) you'd be cured because it was still not understood at the time what was happening as far as these reservoirs. Eventually there was a mathematical model done showing that if someone was on a successful ARV regimen it would take 60 years (@!) to get all the HIV that was slowly coming from these reservoirs.

The above is my very unscientific explanation, the link below discusses some of the latest research on latent HIV in the reservoirs:

actually, the very first genotype I made were showing 4 majors mutations

K103N V108IV M184V T215FIST

With such mutations, I am 100% resistant to the Sustiva (K103N, V108IV) and partially resistant to the Truvada (M184V, T215FIST).

My last unprotected sexual intercourse with my ex gf (the one who infected me) has happen around 6 months min before this first genotype was made.

The first genotype (made in Africa) have shows a subtype C while the 2 others (made in Africa same lab and Europe) a subtype AE.

The polymorphisms between the 2 last genotypes was very similar, but quite differents from those mentioned in the first.

So the 3 reasons to think that the first genotype wasn't mine are:

1) The presence M141V mutation in the first genotype while treatment naive and no other sexual intercourse sinceI left my ex. This mutation should have disappear outside a drug pressure.

2) The contradicting subtype. And no trace of the subtype C: the European lab have done extensive analysis to try to find the subtype C. But no traces. Now the VL was 550 only.

3) The similitudes of the polymorphisms between the two last genotypes (something like 90%), and the differences compared to the first (around 40% of similitude) but no majors mutations showed in the 2 last genotype. Now those 2 genotypes were made around a year later the first one, and the time between the 2nd and 3rd genotypes was of only 3 months.

Based on these considerations, it has been assumed that the first genotype wasn't mine, and that it was worth to start with Atripla.

My VL when I started Atripla was 450. I have been undectectable after 3 weeks, and always since (but again started at 450 VL).

I just have this doubt in my mind that the first genotype could be mine. If the lab have recognize an error in the subtype (wrong algorithm), they still believe this genotype is mine, as the algorithm have no impact on the mutations/polymorphism they have found.

Consequently, I was wondering how long time it will take to fail on Atripla if the first genotype was mine.The "problem" is that as my body was controlling the virus (low VL), I can imagine possible that I am failing partially on Atripla and that my body is able to control the remaining viremia (as the Truvada should partially work).

It's a complex situation, and the only things I can do is to wait for a possible failure.But how long should I wait in order to be able to conclude ?

John

EDIT: minor english corrections, and that's not enough, I know. My crap english. Sorry for that

If I'm reading your question correctly ( How long will it take to fail Atripla ? ) with an undetectable vl and a cd4 count in the 500s even with the partial resistance to truvada, there is no way to tell . If your Doctor keeps good track of your cd4% there should be a tip off as to when the regimen is failing and of course an increase in viral load from undetectable is also a good clue.

The good news is that there are plenty of options open to you if atripla fails. So it is really a waiting game.

I would also mention that taking a genotype with a viral load of 550 is not as reliable as having a vl greater than 1000.

If we assume the graph is representative of a combination of ongoing causes of failure combined with a cluster that has undetected resistance at the beginning, the point at which the curve changes shape would appear to be the median point for time to failure for the group with undetected resistance from the start of therapy. That's consistent with a 1.6 year median cited in a 2006 paper. As a working physicist you probably have better journal access than I, so if still curious try searching: virological failure, resistance, time to failure.

Hope that's a lead to help you satisfy your intellectual curiosity.

But I know that you also have to be concerned, deep down, on a personal basis. And there I think Veritas has pointed out the key item.

None of us that have made it to undetectable really know for sure whether we are undetectable with no HIV replication or whether there is a chance that we have very low level viremia. Nor do our doctors. But you can take steps to manage that low level risk by getting a periodic viral load test. And even if resistance should develop there are many other treatments already and more likely to arrive well before you work your way through what you are on and those already approved.

So the steps you would take to manage this "freak test" risk are the same you would take in any event. Knowing you have done what you can to manage the risk can be freeing, allowing you to spend your energy on the quality of your life.

If you have a strong NNRTI mutation like 103 you are unlikely to reach undetectable eg viral load <50 copies, or stay there more than a few weeks if you do. K103N causes 20-50 fold resistance to the efavirenz in Atripla, ie it stops it working.

CD4 count falling on Atripla .. hmmm, I would like to know where this idea comes from. Look at the results 1 year in and start formulating an opinion. CD4 count should go up, a little, a lot. Since CD4 counts can vary by +/- 50 per test, your two results mean basically the same, a level position.

2) Looking at many CD4 counts here or there for people on Atripla, I believe that it is common to see at the begining of the treatment a slight drop in the CD4 count (but often an increase of the CD4%).Any explanations for that (death of the infected cells ?) ?

Well, I won't speak for what is "common", but I can tell you that my last CD4 without meds was 288 (18%), 3 weeks later I started with Sustiva/Truvada. 2 months after starting my CD4 was 521 (27%). I suppose that it was possible that I dipped before going up, but I'll never know. 3 years later my CD4 is 773 (37%) -- with a high reading in that time of 879.I should point out that I added Reyataz/Norvir 6 months after starting meds because of 41L and 215S mutations -- these decreased the effectiveness of the Truvada and we wanted to "protect" the Sustiva. I am happy as can be with this regimen.

Bottomline -- if you are on an active regimen, your viral load should go down and your CD4s should improve, sometimes slowly, sometimes more quickly.

Wow, after reading John's post, I think I need to attend medical school to understand all of this stuff..ha ha.

I do admit, I am learning at a very high rate of speed. It's funny how extremely motivated you can become in buckling down and learning new things when your longevity depends on it.

You needn't get a medical degree -- you just have to read and learn. Some folks do get far more obsessive about all this and throw around lots of "theories" that can confuse and overwhelm others -- especially when their theories aren't necessarily proven.

So my current regimen. I have been undetectable after 3 weeks and always since (but last lab made 3 weeks ago). I saw an increase of the CD4% of 3%, but my CD4 have remain almost unchanged (slight decrease to 530 for 570).

John: I'm not clear what your VL load was when you started meds for the first time (450?) but if it was a low VL when you started then that could explain the fact that you only had a slight rise in CD4s. According to Dr. Joel Gallant (who I keep quoting because he's so good), when starting therapy for the first time, "The magnitude of the CD4 count increase is correlated with the magnitude of the viral load decline." So if you start treatment with a low VL, it's not expected that CD4s will increase as much as when you start with a high VL.

CD4 count falling on Atripla .. hmmm, I would like to know where this idea comes from. Look at the results 1 year in and start formulating an opinion. CD4 count should go up, a little, a lot. Since CD4 counts can vary by +/- 50 per test, your two results mean basically the same, a level position.

Well, everyone is different. My bf had no resistance like me, and was on atripla his first 9 months of HAART. His initial CD4 count was 230 . It shot up to the 300s, then 400s. Then it abruptly dropped to 200 for no apparent reason - his lowest. He was undetectable the whole time.He switched to Truvada/Norvir/Reyataz for one year. His CD4 counts were a bit more consistent in the 300s. But he had issues with the reyataz - too high bilirubin. So he is back on atripla since december. He hasn't had too many tests since yet. But he is still undetectable.

John: I'm not clear what your VL load was when you started meds for the first time (450?) but if it was a low VL when you started then that could explain the fact that you only had a slight rise in CD4s. According to Dr. Joel Gallant (who I keep quoting because he's so good), when starting therapy for the first time, "The magnitude of the CD4 count increase is correlated with the magnitude of the viral load decline." So if you start treatment with a low VL, it's not expected that CD4s will increase as much as when you start with a high VL.

How low does he define "low" VL ?

FYI here are my bf's history in case anybody cares, much of it on atripla :4/2006 HIV-11/15/2006 HIV+The next couple of tests were done by the county and they didn't give a written record, but this is my recollection :11/30/2006 CD4 300 13% VL 40001/30/2007 CD4 230 9% VL 300003/25/2007 started Atripla . Would have been earlier if the county didn't take so long for the genotype!4/1/2007 I got my old job back, and put him on my Kaiser insurance. Written records from then on. I scan/OCR/backup everything...4/13/2007 CD4 350, 16% VL 1115/17/2007 CD4 263, 14%, VL 856/14/2007 CD4 256 14% VL <757/21/2007 CD4 282 19% VL <7511/12/2007 CD4 203, 18%, VL <7512/2/2007 CD4 361, 15%, VL <75Switched to Norvir/Reyataz/Truvada (not just numbers isssue, but fatigue suspected to be from Sustiva).1/20/2008 CD4 363, 19%, VL<755/2/2008 CD4 365, 21%, VL<758/17/2008 CD4 430, 19%, VL<7511/01/2008 CD4 323, 19%, VL<75Switched back to Atripla due to high bilirubin12/15/2008 CD4 302, 17%, VL<75Looks like it's time for him to go back to the lab now.

I think it's clear that the Atripla wasn't working as well, and CD4 and % were better with the Norvir/Reyataz/Truvada for him. There were several reasons for switching back - the main one being elevated bilirubin. The other is that he was still as fatigued as before on that treatment, so it wasn't the atripla causing it. One more was that the Kaiser pharmacy could never get his meds right with the 3 meds, so he preferred to get his treatment in 1 pill. And the last one was that Norvir had to be refrigerated and that was a big pain especially when traveling.

Now Kaiser sends him his Atripla in the mail each month automatically, free under ADAP, no more pharmacy problems. But they couldn't have done that with the Norvir due to refrigeration.

That's a good question. He thought mine was low at 9k as far as indicating not a huge CD4 rise after starting. He pretty much said that having a low VL when beginning treatment was not a guarantee that your CD4s would not have a huge rise but, in general, that's what's been observed to happen.

I think it's clear that the Atripla wasn't working as well, and CD4 and % were better with the Norvir/Reyataz/Truvada for him. There were several reasons for switching back - the main one being elevated bilirubin. The other is that he was still as fatigued as before on that treatment, so it wasn't the atripla causing it. One more was that the Kaiser pharmacy could never get his meds right with the 3 meds, so he preferred to get his treatment in 1 pill. And the last one was that Norvir had to be refrigerated and that was a big pain especially when traveling.

So, let's be clear -- the Atripla or the Reyataz/Norvir/Truvada does not directly impact the CD4s. The job of these meds is to take out the virus. With the virus under control, the CD4's are able to come back because the virus is no longer using them as HIV factories.This is why many doctors (including Dr. Gallant), tells folks to focus on CD4's before treatment and to focus on VL once treatment is begun.

So, let's be clear -- the Atripla or the Reyataz/Norvir/Truvada does not directly impact the CD4s. The job of these meds is to take out the virus. With the virus under control, the CD4's are able to come back because the virus is no longer using them as HIV factories.This is why many doctors (including Dr. Gallant), tells folks to focus on CD4's before treatment and to focus on VL once treatment is begun.

Well, both meds were doing the job of suppressing the virus below 75 copies/ml. Maybe with a more precise test we could tell if one was doing a better job.

But I think it's still interesting that my bf's CD4s were higher with one combo vs the other when both were suppressing the virus below 75 copies.

Thanks for the link !The study you are mentioning give the following numbers:

For those who started with an NNRTI regimen, the probability of switching to a PI was 11% by 2 years, 18% by 4 years and 26% by 6 years.

For those who started with a regimen containing a single PI, the probability of switching to an NNRTI was 27% by 2 years, 51% by 4 years and 61% by 6 years.

For those who started with a regimen containing a PI with ritonavir, the probability of switching to an NNRTI was 27% by 2 years and 42% by 4 years.

Finally, for those who started with abacavir with two other nucleosides the probability of switching to an NNRTI or a PI was 29% by 2 years and 35% by 4 years.

Means the cumulative odds to switch from an NNRTI regimen to a PI was 55% by 6 years.Sounds like the 50% are around 5 years. Where come from the 1.6 years and for how many percent of people ? Or maybe are you saying that the first failure seems to appears in average after 1.6 years ?

The graph you have post seems to shows that the first virological failures have appear after 6 months, if we look at where the viral load failure curve start to go above zero.

Thanks for your tips. Focusing on the quality of life after having do our own best is definitely what I should do, and am doing I was just wondering if I should go every month to the lab (to see if there was a failure) or if I could wait like most of us 3 months, which is not a good idea as the longer we stay on a failing regimen, the worst become the life expectancy.

So I was willing to know after how long one get a virologic failure, in average.I am starting to considere 6-9 months as being a good start.

newtIf you have a strong NNRTI mutation like 103 you are unlikely to reach undetectable eg viral load <50 copies, or stay there more than a few weeks if you do. K103N causes 20-50 fold resistance to the efavirenz in Atripla, ie it stops it working.

Very interesting. Do you know up to how many weeks typically ?Do you think a low increase in the CD4 despite undetectable could means that some drugs are not fully working and that the 4th drug is the body ?

CD4 count falling on Atripla .. hmmm, I would like to know where this idea comes from. Look at the results 1 year in and start formulating an opinion. CD4 count should go up, a little, a lot. Since CD4 counts can vary by +/- 50 per test, your two results mean basically the same, a level position.

Got it. I took a llok to the signature of many in this website to make my assertion, but how meaningless is that ? Your approach sounds more appropriate.

newt your posts are always very helpful, thanks for your help !

Inchlingblue

"The magnitude of the CD4 count increase is correlated with the magnitude of the viral load decline." So if you start treatment with a low VL, it's not expected that CD4s will increase as much as when you start with a high VL.

It's very intriguing beacause many studies have shows that those starting earlier have the best chance to get the greater CD4 increase, while others studies have mention that the lower was the VL at the begining of the treatment, the longer the combo (assuming no resistances) will be likely to work.

But never I have heard that starting with a low VL could implie a low increase in the CD4 count.Now it make sens also.

The job of these meds is to take out the virus. With the virus under control, the CD4's are able to come back because the virus is no longer using them as HIV factories.

This is why many doctors (including Dr. Gallant), tells folks to focus on CD4's before treatment and to focus on VL once treatment is begun.

Wonderful tip ! Really. Now, I also agree with madbrain but the arguments are conflicting no ?But you are probably both right no ?If the drugs might not probably be helping to stimulate the production of lymphocytes, some regimen might not be fully suppressive despite one is undetectable.So switching to another regimen might result in a bigger CD4 increase.Now, the CD4 count doesn't seem to be a good predictor of a virologic failure.

madbrain

Well, both meds were doing the job of suppressing the virus below 75 copies/ml. Maybe with a more precise test we could tell if one was doing a better job.

But I think it's still interesting that my bf's CD4s were higher with one combo vs the other when both were suppressing the virus below 75 copies.

I heard from ID docs that switching to a new regimen can lead to a much better CD4 increase.

Now can they be predictor/clue of a virologic failure as you have mention, I don't know.That was my point. Also to know if there is a study about that.

So far, my CD4 have increase by 3%. So if you are right, so far so good.

John

EDIT:

This study conclude as follow about the CD4 count (but nothing about the CD4%)

CD4 count changes correlated significantly with VL at group level but had very limited utility in identifying virological failure in individual patients. CD4 count is an inadequate alternative to VL measurement for early detection of virological failure.

For those who started with an NNRTI regimen, the probability of switching to a PI was 11% by 2 years, 18% by 4 years and 26% by 6 years.

For those who started with a regimen containing a single PI, the probability of switching to an NNRTI was 27% by 2 years, 51% by 4 years and 61% by 6 years.

For those who started with a regimen containing a PI with ritonavir, the probability of switching to an NNRTI was 27% by 2 years and 42% by 4 years.

Finally, for those who started with abacavir with two other nucleosides the probability of switching to an NNRTI or a PI was 29% by 2 years and 35% by 4 years.

Means the cumulative odds to switch from an NNRTI regimen to a PI was 55% by 6 years.Sounds like the 50% are around 5 years. Where come from the 1.6 years and for how many percent of people ? Or maybe are you saying that the first failure seems to appears in average after 1.6 years ?

The graph you have post seems to shows that the first virological failures have appear after 6 months, if we look at where the viral load failure curve start to go above zero.

Thanks for your tips. Focusing on the quality of life after having do our own best is definitely what I should do, and am doing I was just wondering if I should go every month to the lab (to see if there was a failure) or if I could wait like most of us 3 months, which is not a good idea as the longer we stay on a failing regimen, the worst become the life expectancy.

So I was willing to know after how long one get a virologic failure, in average.I am starting to considere 6-9 months as being a good start.

Hi JohnThe analysis in the paper of people switching regimens is unfortunately not relevant to the question of virological failure since people switch for a variety of reasons -- those switching due to virological failure would be a subset of those switching for all reasons.

The main point however is that it is a distribution rather than a set time at which resistance arises-- and that the way to manage a risk of that nature is through periodic monitoring. Not sure why you would need to monitor monthly however, every 3 months seems to be standard of care at first, gradually extending to 4 or even 6 months once results are stable.

I feel like I should take a college course to learn about this, and I really want to know. haha. So many acronyms and what not. My Dr is big on education and I'm just so thankful for all the people on here with info, but I'm going to have to read this several times.

CD4 cell tests are normally reported as the number of cells in a cubic millimeter of blood, or mm3. Normal counts are between 500 and 1600. CD4 counts drop gradually in people with HIV. However, in some cases they can drop quickly. Because the CD4 cell counts are so variable, some health care providers prefer to look at the CD4 cell percentages. These percentages refer to total lymphocytes. If your test reports CD4% = 34%, that means that 34% of your lymphocytes were CD4 cells. This percentage is more stable than the number of CD4 cells. The normal range is between 20% and 40%.

A CD4 count below 200 or a CD4 percentage below 14% indicates serious immune damage. It is a sign of AIDS in people with HIV infection. A recent study showed that the CD4% is a better predictor of HIV disease progression than the CD4 count. However, the CD4 count is used to decide when to start treatment.

Not to pile on, but where did "The normal range is between 20% and 40%" come from?

My lab report shows a reference / normal range for CD4 % of 30.8% to 58.5%, about 50% higher than the numbers above.

Reference ranges for tests can differ, and frequently do, from lab to lab. A laboratory SHOULD create reference ranges based on their population -- this, combined with any potential differences in testing methodology can account for small to larger differences in these ranges. For instance, a normal range for RBC in a lab that is located at sea level, should have a lower reference range than a lab in Denver (mile high city), because the decrease in oxygen levels in Denver should cause an increased RBC count in the general population.So.... while I agree these two ranges seem quite different, it is dangerous to assume that your lab's reference range is applicable everywhere.

It's a moot point, CD4 v CD4%. The Italian study is more up to date. Ideally you wanna look at the trend in both and pay attention to counts that don't match the related % (and vice versa). Me personally, I would go by count unless % was low and count was high - matt

Reference ranges for tests can differ, and frequently do, from lab to lab. A laboratory SHOULD create reference ranges based on their population -- this, combined with any potential differences in testing methodology can account for small to larger differences in these ranges. For instance, a normal range for RBC in a lab that is located at sea level, should have a lower reference range than a lab in Denver (mile high city), because the decrease in oxygen levels in Denver should cause an increased RBC count in the general population.So.... while I agree these two ranges seem quite different, it is dangerous to assume that your lab's reference range is applicable everywhere.

Mike

I agree that there can be differences in lab report reference ranges -- actually that's why I specified it was a specific lab report reference range.

But those differences are generally minor, especially in terms of percentages.

The lessons on this site suggest a normal range of 32% to 68% versus Labcorp's 30.8% to 58.5% -- that's the type of range of variation that sounds more likely. Veritas' numbers are inconsistent by a big margin (two thirds the other numbers). Thus it would be a good idea to look at the source to see whether it is credible or was instead talking about something else.

I agree that there can be differences in lab report reference ranges -- actually that's why I specified it was a specific lab report reference range.

But those differences are generally minor, especially in terms of percentages.

The lessons on this site suggest a normal range of 32% to 68% versus Labcorp's 30.8% to 58.5% -- that's the type of range of variation that sounds more likely. Veritas' numbers are inconsistent by a big margin (two thirds the other numbers). Thus it would be a good idea to look at the source to see whether it is credible or was instead talking about something else.

I agree that the difference stated here seemed high, but I have seen far greater differences in reference ranges. The bottomline is really this -- the ONLY reference range that anyone should be concerned with, is the reference reported WITH your lab result.

"...health will finally be seen not as a blessing to be wished for, but as a human right to be fought for." Kofi Annan

Nymphomaniac: a woman as obsessed with sex as an average man. Mignon McLaughlin

HIV is certainly character-building. It's made me see all of the shallow things we cling to, like ego and vanity. Of course, I'd rather have a few more T-cells and a little less character. Randy Shilts

Thanks Veritas -- basically looks like they all link back to an AIDSInfonet fact sheet (#124) that specifies a range of 20% to 40%.But they do not cite to any published paper etc.

And they still have the same point for likely AIDS (around 14%)

And the numbers are suspiciously round.

Sounds fishy...

Mike and Ann have presented rationales for why it is conceivable the number is correct (although the fact they are denoted in percentages and cover such a broad range and that both are presented as generic US numbers makes those arguments less powerful than they would otherwise be). So let's ask: Does anyone reading this actually have a lab report that shows a 20% to 40% reference range for CD4 percent? If so, what was the lab?

Reference ranges for tests can differ, and frequently do, from lab to lab. A laboratory SHOULD create reference ranges based on their population -- this, combined with any potential differences in testing methodology can account for small to larger differences in these ranges. For instance, a normal range for RBC in a lab that is located at sea level, should have a lower reference range than a lab in Denver (mile high city), because the decrease in oxygen levels in Denver should cause an increased RBC count in the general population.So.... while I agree these two ranges seem quite different, it is dangerous to assume that your lab's reference range is applicable everywhere.

Again, this really comes back to the definition of "normal". You could have a lab in an HIV clinic where the average ranges would be quite different from the rest of the (HIV-) population. I wouldn't want that lab to show me a "normal" range based on their patient population alone. It wouldn't be very helpful. I think one needs to take more data points than just a few local ones to come up with "normal" averages. It's legitimate to use a large data set, say, statewide or nationwide, even if there is a bit of local variance.

The values appear at the end ----- range 30.13 to 60.23 in healthy adults. I can't find where the body came up with 20 to 40. However, a study must exist because I don't think they would all be quoting that value on a whim. Since my own lab's ranges are 31 - 60, I'll stick with that. Although the 20 to 40 numbers would make my 38% look wonderful.

Again, this really comes back to the definition of "normal". You could have a lab in an HIV clinic where the average ranges would be quite different from the rest of the (HIV-) population. I wouldn't want that lab to show me a "normal" range based on their patient population alone. It wouldn't be very helpful. I think one needs to take more data points than just a few local ones to come up with "normal" averages. It's legitimate to use a large data set, say, statewide or nationwide, even if there is a bit of local variance.

Two points:

1 - It is risky to refer to a reference range as a "normal range". What is abnormal for one person, may be quite normal for another. Additionally, a "normal" result for a test may not be so normal if looked at with other test results. A reference range is simply that -- a range that your doctor can use when interpreting your test results. The determination of whether it is "normal" for you is based on the result of that test, your history and any other info that the doctor has at his/her hand.2 - A reference range for a test SHOULD be based on "healthy" individuals (yes, this can be tricky and risky). I would not expect any KNOWN HIV+ individuals to be included in the development of reference ranges for CD4 tests

So -- the reality is most large labs do use quite a large data set to establish ranges -- and smaller labs will often use some range from either a larger reference lab, where they may send some testing, or some other source of a reference range based on similar testing methodology.

Again -- the only reference range of interest to anyone is the one supplied with your actual lab result.

Thanks Veritas -- basically looks like they all link back to an AIDSInfonet fact sheet (#124) that specifies a range of 20% to 40%.But they do not cite to any published paper etc.

And they still have the same point for likely AIDS (around 14%)

And the numbers are suspiciously round.

Sounds fishy...

Mike and Ann have presented rationales for why it is conceivable the number is correct (although the fact they are denoted in percentages and cover such a broad range and that both are presented as generic US numbers makes those arguments less powerful than they would otherwise be). So let's ask: Does anyone reading this actually have a lab report that shows a 20% to 40% reference range for CD4 percent? If so, what was the lab?

(We'll have to find a suitable prize )

My lab (Quest Diagnostics -- in North Carolina), has a reference range of 30%-61% for CD4%.

A range that has the high end 100% higher than the low end, tells me that it is an assay with quite a bit of variation in the general (and assumed healthy) population.

Mike(who hopes that he gets some prize for a range that encompasses part of the requested 20-40% - )

The values appear at the end ----- range 30.13 to 60.23 in healthy adults. I can't find where the body came up with 20 to 40. However, a study must exist because I don't think they would all be quoting that value on a whim. Since my own lab's ranges are 31 - 60, I'll stick with that. Although the 20 to 40 numbers would make my 38% look wonderful.

veritas

Incidently, my Kaiser labs shows the normal CD4% range as 30 to 60%, and I live right next to San Jose.

1 - It is risky to refer to a reference range as a "normal range". What is abnormal for one person, may be quite normal for another. Additionally, a "normal" result for a test may not be so normal if looked at with other test results. A reference range is simply that -- a range that your doctor can use when interpreting your test results. The determination of whether it is "normal" for you is based on the result of that test, your history and any other info that the doctor has at his/her hand.

A range is, by definition, not personalized. That said, Kaiser use the very words "normal range" in the printouts for every lab results they mail. They even have a column full of those ranges for each type of the test. It is not just for the doctor's use, but for patient use as well.

A range is, by definition, not personalized. That said, Kaiser use the very words "normal range" in the printouts for every lab results they mail. They even have a column full of those ranges for each type of the test. It is not just for the doctor's use, but for patient use as well.

Well, then I can tell you that Kaiser's lab is not following common industry practice. The term "normal range" should have been replace years ago. To be clear -- I have a BS degree in Medical Technology and worked in clinical labs for more than a dozen years (although not at this time), so I'm speaking from experience and education here.You are correct that ranges are not "personalized", but people tend to lose sight of that when it pertains to them.While you are correct, ranges are for patient to use as well -- it can be dangerous for a patient to start interpreting results (in general) without being able to look at the WHOLE picture. It is far to easy for someone with a hugely vested interest to NOT focus on a "out of range" result and begin to worry/panic (again, not all, but many...). A doctor can take a more logical approach without the emotions of fear -- not to mention they have the training to NOT be thrown simply by an "off" result. Hell, I even have a hard time myself -- and I have a little more education than most on the interpretation of laboratory results.When I was working in labs back in Mass and RI in the 80's and 90's -- it was against policy (and the law in RI) for a lab to give results to anyone other than a clinician. I know this is changing all over now -- I think it is a good change, but one fraught with risk.

I understand your concern with releasing lab info to patients and I also agree with you that it is a cautionary good thing. With the advent of the internet, patients can be very well informed with respect to their health issues if they are willing to do the necessary research. The problem is: " Does the patient know how to do the appropriate research?" "Will the patient have the where with all to ask their Dr. the appropriate questions?" And of course: Will their Dr. be receptive ?" ( I know what you and I would do if they weren't. LOL ) Bottom line for me, It is always better to know. I have to admit I've obsessed on an out of range result, but the more research I do the less concerned I become with a one-off oddity. I believe the UK requires that all medical documents be released to the patient by law including Dr.'s notes . I hope we are going in that direction. It keeps everyone honest.

By the way ,Quest Diagnostics is a great lab. I believe when geno's and pheno' first came out a lot of labs sent blood their for evaluation. Do you have a web site for them that shows their lab ranges? Would be much obliged! (How's that for cowboy talk?) Thanks.